Unlike Sun1−/−Sun2−/− or Syne1−/−Syne2−/− mice, which suffer from defective neocortical lamination and fail to thrive after birth (Zhang et al., 2009), the viable Sun1−/− and Sun−/−Sun2+/− animals, which present with cerebellar ataxia, might serve as a working model for the study of the molecular mechanisms underlying SYNE1-associated ARCA1 (Dupré et al., 2007; Gros-Louis et al., 2007), as well as for the identification of therapeutic targets in neurodegenerative diseases involving Purkinje cell loss (Millen and Gleeson, 2008). This evidence concerns the gene SYNE1 and neurodegenerative disease.